scholarly journals Sevoflurane post-conditioning increases nuclear factor erythroid 2-related factor and haemoxygenase-1 expression via protein kinase C pathway in a rat model of transient global cerebral ischaemia

2015 ◽  
Vol 114 (2) ◽  
pp. 307-318 ◽  
Author(s):  
H. Lee ◽  
Y.H. Park ◽  
Y.T. Jeon ◽  
J.W. Hwang ◽  
Y.J. Lim ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Rat Model ◽  
Cerebral Ischaemia ◽  
Related Factor ◽  
Nuclear Factor ◽  
Kinase C ◽  
Global Cerebral Ischaemia

scholarly journals Propofol Inhibits Ischemia/Reperfusion-Induced Cardiotoxicity Through the Protein Kinase C/Nuclear Factor Erythroid 2-Related Factor Pathway

2021 ◽  
Vol 12 ◽  
Author(s):  
Shengqiang Li ◽  
Zhen Lei ◽  
Meng Zhao ◽  
Yonghao Hou ◽  
Di Wang ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Ischemia Reperfusion ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Nuclear Factor ◽  
H9c2 Cells ◽  
Nrf2 Pathway ◽  
Kinase C ◽  
Creatine Kinase Mb

Both hydrogen peroxide (H2O2, H) and ischemia/reperfusion (I/R) can damage cardiomyocytes, which was inhibited by propofol (P). The present research was designed to examine whether propofol can reduce myocardial I/R injury by activating protein kinase C (PKC)/nuclear factor erythroid-2-related factor 2 (NRF2) pathway in H9C2 cells and rat Langendorff models. H9C2 cells were disposed of no reagents (C), H2O2 for 24 h (H), propofol for 1 h before H2O2 (H+P), and chelerythrine (CHE, PKC inhibitor) for 1 h before propofol and H2O2 (H+P+CHE). N = 3. The PKC gene of H9C2 was knocked down by siRNA and overexpressed by phorbol 12-myristate 13-acetate (PMA, PKC agonist). The cell viability and the expressions of PKC, NRF2, or heme oxygenase-1(HO-1) were evaluated. Propofol significantly reduced H9C2 cell mortality induced by H2O2, and significantly increased NRF2 nuclear location and HO-1 expression, which were restrained by siRNA knockout of PKC and promoted by PMA. Rat hearts were treated with KrebsHenseleit solution for 120 min (C), with (I/R+P) or without (I/R) propofol for 20 min before stopping perfusion for 30 min and reperfusion for 60 min, and CHE for 10 min before treated with propofol. N = 6. The levels of lactate dehydrogenase (LDH), superoxide dismutase (SOD), and creatine kinase-MB (CK-MB) in perfusion fluid and antioxidant enzymes in the myocardium were assessed. I/R, which increased LDH and CK-MB expression and reduced SOD expression, boosted the pathological damage and infarcts of the myocardium after reperfusion. However, propofol restrained all these effects, an activity that was antagonized by CHE. The results suggest that propofol pretreatment protects against I/R injury by activating of PKC/NRF2 pathway.

scholarly journals Activation of Nuclear Factor κB (NF-κB) in Prostate Cancer Is Mediated by Protein Kinase C ϵ (PKCϵ)

2012 ◽  
Vol 287 (44) ◽  
pp. 37570-37582 ◽  
Author(s):  
Rachana Garg ◽  
Jorge Blando ◽  
Carlos J. Perez ◽  
HongBin Wang ◽  
Fernando J. Benavides ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Kinase C

scholarly journals Inhibition of protein kinase C beta phosphorylation activates nuclear factor-kappa B and improves postischemic recovery in type 1 diabetes

2020 ◽  
Vol 245 (9) ◽  
pp. 785-796
Author(s):  
Satyanarayana Alleboina ◽  
Thomas Wong ◽  
Madhu V Singh ◽  
Ayotunde O Dokun
Keyword(s):  
Endothelial Cells ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
High Glucose ◽  
Nuclear Factor Kappa B ◽  
Nuclear Factor ◽  
Nuclear Factor Kappa ◽  
Kinase C ◽  
Protein Kinase C Beta

Peripheral artery disease (PAD) is a major health problem and is caused by atherosclerosis in arteries outside the heart leading to impaired blood flow. The presence of diabetes significantly increases the likelihood of having worse outcomes in PAD, and the molecular mechanisms involved are poorly understood. Hyperglycemia in diabetes activates the nuclear factor-kappa B (NF-κB) pathway, and chronic inflammation in diabetes is associated with vascular complications. Ischemia also activates NF-κB signaling that is important for perfusion recovery in experimental PAD. We hypothesized that prolonged exposure of endothelial cells to high glucose in diabetes impairs ischemic activation of the NF-κB pathway and contributes to poor perfusion recovery in experimental PAD. We assessed the effect of high glucose and ischemia on canonical and non-canonical NF-κB activation in endothelial cells and found both conditions activate both pathways. However, exposure of endothelial cells to high glucose impairs ischemia-induced activation of the canonical NF-κB pathway but not the non-canonical pathway. We probed an array of antibodies against signaling proteins in the NF-κB pathway to identify proteins whose phosphorylation status are altered in endothelial cells exposed to high glucose. Protein kinase C beta (PKCβ) was among the proteins identified, and its role in impaired ischemia-induced activation of NF-κB during hyperglycemia has not been previously described. Inhibition of PKCβ improves ischemia-induced NF-κB activation in vitroand in vivo. It also improves perfusion recovery in diabetic mice following experimental PAD. Thus, in diabetes, PKCβ phosphorylation contributes to impaired ischemic activation of NF-κB and likely a mechanism contributing to poor PAD outcomes. Impact statement Diabetes worsens the outcomes of peripheral arterial disease (PAD) likely in part through inducing chronic inflammation. However, in PAD, recovery requires the nuclear factor-kappa B (NF-κB) activation, a known contributor to inflammation. Our study shows that individually, both ischemia and high glucose activate the canonical and non-canonical arms of the NF-κB pathways. We show for the first time that prolonged high glucose specifically impairs ischemia-induced activation of the canonical NF-κB pathway through activation of protein kinase C beta (PKCβ). Accordingly, inhibition of PKCβ restores the ischemia-induced NF-κB activity both in vitroin endothelial cells and in vivoin hind limbs of type 1 diabetic mice and improves perfusion recovery after experimental PAD. Thus, this study provides a mechanistic insight into how diabetes contributes to poor outcomes in PAD and a potential translational approach to improve PAD outcomes.

scholarly journals Rho Kinase and Protein Kinase C Pathways are Responsible for Enhanced Carbachol Contraction in Permeabilized Detrusor in a Rat Model of Cystitis

2018 ◽  
Vol 123 (5) ◽  
pp. 567-576
Author(s):  
Merve Denizalti ◽  
Nezahat Tugba Durlu-Kandilci ◽  
Gul Simsek ◽  
Turgut Emrah Bozkurt ◽  
Inci Sahin-Erdemli
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Rat Model ◽  
Rho Kinase ◽  
Kinase C
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